# Predicting Neuromodulation Outcome for Parkinson's Disease with Generative Virtual Brain Model

arXiv: https://arxiv.org/abs/2603.29176 · HTML: https://mlsanity.com/paper/2603.29176/

## Key facts

- No citing papers in the map yet (data through 14 Oct 2026).
- Builds on 7 of its 51 references that are in the map.
- First posted on arXiv 31 Mar 2026.

## Builds on (most cited first, 7 of 7)

- [Semi-Supervised Classification with Graph Convolutional Networks](https://mlsanity.com/paper/1609.02907/) (2016)
- [Qwen3 Technical Report](https://mlsanity.com/paper/2505.09388/) (2025)
- [On the Opportunities and Risks of Foundation Models](https://mlsanity.com/paper/2108.07258/) (2021)
- [Large Language Models Encode Clinical Knowledge](https://mlsanity.com/paper/2212.13138/) (2022)
- [OpenAI GPT-5 System Card](https://mlsanity.com/paper/2601.03267/) (2025)
- [Prefix Conditioning Unifies Language and Label Supervision](https://mlsanity.com/paper/2206.01125/) (2022)
- [Mapping effective connectivity by virtually perturbing a surrogate brain](https://mlsanity.com/paper/2301.00148/) (2022)

## Abstract (arXiv)

Parkinson's disease (PD) affects over ten million people worldwide. Although temporal interference (TI) and deep brain stimulation (DBS) are promising therapies, inter-individual variability limits empirical treatment selection, increasing non-negligible surgical risk and cost. Previous explorations either resort to limited statistical biomarkers that are insufficient to characterize variability, or employ AI-driven methods which is prone to overfitting and opacity. We bridge this gap with a pretraining-finetuning framework to predict outcomes directly from resting-state fMRI. Critically, a generative virtual brain foundation model, pretrained on a collective dataset (2707 subjects, 5621 sessions) to capture universal disorder patterns, was finetuned on PD cohorts receiving TI (n=51) or DBS (n=55) to yield individualized virtual brains with high fidelity to empirical functional connectivity (r=0.935). By constructing counterfactual estimations between pathological and healthy neural states within these personalized models, we predicted clinical responses (TI: AUPR=0.853; DBS: AUPR=0.915), substantially outperforming baselines. External and prospective validations (n=14, n=11) highlight the feasibility of clinical translation. Moreover, our framework provides state-dependent regional patterns linked to response, offering hypothesis-generating mechanistic insights.